The first two stages of the disease have a good prognosis. Stage three and four have a poor prognosis.
Call your provider if you or people around you notice any problems with your mental state or nervous system function. This is important for people who already have a liver disorder. HE can get worse quickly and become an emergency condition. Treating liver problems may prevent HE. Avoiding heavy drinking and intravenous drug use can prevent many liver disorders. Ferri FF. Hepatic encephalopathy. In: Ferri FF, ed. Ferri's Clinical Advisor Philadelphia, PA: Elsevier; Garcia-Tsao G. Cirrhosis and its sequelae. Goldman-Cecil Medicine. Philadelphia, PA: Elsevier Saunders; chap Jakhete N, Kim AK.
The management of hepatic encephalopathy. Current Surgical Therapy. Hepatic encephalopathy, hepatorenal syndrome, hepatopumonary syndrome, and other systemic complications of liver disease. Essence of Anesthesia Practice. Updated by: Michael M. Editorial team. Loss of brain function - liver disease. HE can occur suddenly and you may become ill very quickly. Causes of HE may include: Hepatitis A or B infection uncommon to occur this way Blockage of blood supply to the liver Poisoning by different toxins or medicines Constipation Upper gastrointestinal bleeding People with severe liver damage often suffer from HE.
Early symptoms may be mild and include: Breath with a musty or sweet odor Changes in sleep patterns Changes in thinking Mild confusion Forgetfulness Personality or mood changes Poor concentration and judgment Worsening of handwriting or loss of other small hand movements Severe symptoms may include: Abnormal movements or shaking of hands or arms Agitation, excitement, or seizures occur rarely Disorientation Drowsiness or confusion Behavior or personality changes Slurred speech Slowed or sluggish movement People with HE can become unconscious, unresponsive, and possibly enter a coma.
People are often not able to care for themselves because of these symptoms. Exams and Tests. Signs of nervous system changes may include: Shaking of the hands "flapping tremor" when trying to hold arms in front of the body and lift the hands Problems with thinking and doing mental tasks Signs of liver disease , such as yellow skin and eyes jaundice and fluid collection in the abdomen ascites Musty odor to the breath and urine Tests done may include: Complete blood count or hematocrit to check for anemia CT scan of the head or MRI EEG Liver function tests Prothrombin time Serum ammonia level Sodium level in the blood Potassium level in the blood BUN blood urea nitrogen and creatinine to see how the kidneys are working.
Treatment of HE depends upon the cause. If changes in brain function are severe, a hospital stay may be needed.
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Ammonia is predominantly generated in the gut by intestinal bacteria and enzymes and detoxified primarily in the liver. Since the s, ammonia has been identified as the principal culprit in hepatic encephalopathy HE. Many physicians utilize serum ammonia to diagnose, assess severity, and determine the resolution of HE in patients with chronic liver disease CLD despite research showing that ammonia levels are unhelpful in all of these clinical circumstances.
HE in patients with CLD is a clinical diagnosis of exclusion that should not be based on ammonia levels. A year-old man diagnosed with cirrhosis due to Hepatitis C and alcoholism was brought to the emergency department for alteration in mentation.
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He had scant melenic stools 5 days preceding his admission and did not exhibit overt signs or symptoms of infection. His systemic examination was normal except for somnolence, disorientation to space and time, asterixis, and ascites. His lab parameters were within normal limits except for an elevated blood urea nitrogen and thrombocytopenia. His blood cultures did not grow any organisms, and paracentesis ruled out spontaneous bacterial peritonitis. During his hospital stay, he underwent esophageal variceal banding and was effectively managed with lactulose and rifaximin.
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The patient was alert, fully oriented, and without asterixis at the time of discharge 6 days later. Would an elevated venous ammonia level at admission alter management? If the ammonia level was elevated, would serial ammonia measurements affect management?
The colonic microbiome produces ammonia from dietary nitrogen. The process of transamination and the urea cycle prevents this metabolic product from accumulating in the body. This hyperammonemia is compounded by reduced peripheral metabolism of ammonia by muscle as a consequence of cachexia and muscle atrophy.
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Astrocytes synthesize glutamine excessively in the setting of hyperammonemia, resulting in astrocyte swelling and the generation of reactive oxygen species. Astrocyte swelling, free radical generation, and increased inhibitory function of gamma-Aminobutyric Acid result in cerebral dysfunction.
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The ammonia hypothesis posits that ammonia is key in the pathogenesis of HE. Given these associations between HE and ammonia, physicians have for decades tested serum ammonia levels to diagnose HE and chart its resolution. Multiple factors affect the accuracy of ammonia levels. First, fist clenching or the use of a tourniquet during the process of phlebotomy can falsely increase ammonia levels. Kramer et al.
However, Nicolao et al. Third, ammonia levels are dependent on the time to processing of the specimen. Inaccurate results may occur if the blood sample is not immediately placed on ice after collection or if it is not centrifuged within 15 minutes of collection.